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Poor responses to insulin have been closely associated with Alzheimer’s disease in humans, and previous research has shown that bottlenose dolphins can also develop insulin resistance. That, combined with the recent discovery of amyloid plaques and tangled clumps of fibers in bottlenose dolphin brains, led the researchers to believe that dolphins, like us, may develop signs of Alzheimer’s disease as a result of high levels of blood sugar and insulin.

Research from the Universities of Dundee and Oxford has shown how combining the tetanus vaccine with a viral particle that normally affects cucumbers can be used to treat psoriasis and allergies, and may even protect against Alzheimer’s disease.

Dr. Debbie Toiber, of the BGU Department of Life Sciences, and her team discovered that a specific protein — Sirtuin-6 (SIRT6) — is severely reduced in the brains of Alzheimer’s patients. SIRT6 is critical to the repair of DNA, the deterioration of which “is the beginning of the chain that ends in neurodegenerative diseases in seniors,” she explains.

The blood-brain barrier prevents us from simply being able to inject the protein into the brain to replenish its supply. Dr. Toiber is currently working on finding a way to increase the expression of the protein into the brain.

Ionis and Biogen are bringing to bear the Ionis drug technology called antisense, which targets diseases processes at the genetic level. It blocks or modifies production of proteins involved in disease.

The Phase 1/2a study of the Alzheimer’s drug, IONIS-MAPTRx, seeks evidence of safety and signs of activity. It’s to be given in 44 patients with mild Alzheimer’s over three months.The drug targets microtubule-associated tau protein, also called MATP, or tau, an abnormal protein associated with Alzheimer’s.

“Alzheimer’s disease starts in the brain more than twenty years before the first symptom,” said Richard Isaacson, director of the Alzheimer’s Prevention Clinic at New York-Presbyterian/Weill-Cornell Medical Center. “Alzheimer’s disease is not an older person’s disease. It’s a disease of younger and middle-aged people. And that’s how we have to shift the paradigm.”

As a first step, a team is testing whether it’s possible to stop or slow tau-driven neuron loss and inflammation by lowering ApoE in the early life of laboratory rodents. This scheme mimics a human scenario better than the recent study, which analyzed mice that express or lack APOE from birth. “The implication here, with the recent tau findings, is that you’d really block the neurodegeneration that leads to cognitive decline,” Holtzman says.

In the largest and most conclusive study of its kind, researchers have analysed blood samples to create a novel and non-invasive way of helping to diagnose Alzheimer’s disease and distinguishing between different types of neurodegenerative disorders.

Following this breakthrough discovery, Alzheimer’s sufferers may now have an additional test to improve the accuracy of diagnosis in order to better tailor appropriate treatment. The research also offers a valuable opportunity to monitor the disease.

There is a small but unique study to see if jogging memories where they were made can help older African-Americans stay mentally sharp and slow early memory loss. The link for today has the whole story.

Nearly three dozen new Alzheimer’s drugs may reach the market in the next five years, researchers say.

That includes 27 drugs in phase 3 clinical trials, which are later in the drug review process. It also includes eight drugs in phase 2 clinical trials, according to an analysis by ResearchersAgainstAlzheimer’s (RA2) investigators, an UsAgainstAlzheimer’s network.

Changiz Geula, a professor of neuroscience at Northwestern University, has been studying brain tissue collected from people who died at age 90 or older. He found that some people who die with sharp minds have brains that are clogged with the gunk associated with Alzheimer’s pathology. That means it’s possible to have an “Alzheimer’s brain” but no dementia. Dr. Geula believes that in cases like this, some actor in the brain — call it the opposite of Alzheimer’s — is protecting neurons from damage. We still don’t know what it is.

The National Institute on Aging has created a 44-page booklet with a checklist to make each room in the home a safer environment for someone with dementia. Alzheimer’s progresses differently in each person, but here are some general principles that may be helpful to everyone who is going to be involved in your alzheimer’s care.

Researchers may have uncovered the critical missing piece that could lead to new treatments for Alzheimer’s and other neurodegenerative diseases. It’s an enzyme that plays a role in how the disease develops, but could also be harnessed to work against the tangled accumulation of proteins that eventually wreak havoc in the brains of Alzheimer’s patients.

At MUSIC & MEMORY℠, they help people in nursing homes and other care organizations who suffer from a wide range of cognitive and physical challenges to find renewed meaning and connection in their lives through the gift of personalized music.

Memory performance decreases with increasing age. Cannabis can reverse these ageing processes in the brain. This was shown in mice by scientists at the University of Bonn with their colleagues at The Hebrew University of Jerusalem (Israel). Old animals were able to regress to the state of two-month-old mice with a prolonged low-dose treatment with a cannabis active ingredient. This opens up new options, for instance, when it comes to treating dementia. The results are now presented in the journal Nature Medicine.

See the innovative approach Carlijn Valk, a Dutch Industrial Designer working on her Ph.D. has used to bring nature closer to elderly patients with dementia and how it has helped them feel positive and think back about their past experiences.

The joint effort, known as the Alzheimer’s Combination Therapy Opportunities (ACTO) grant initiative, will provide $2 million this year for testing approaches that simultaneously target two or more processes believed to underlie, exacerbate, or occur in the disease.

IN short: New findings indicate that the induction of metaplasticity by ryanodine receptor activation contributes to the reestablishment of plasticity and associativity in hippocampal neurons of APP/PS1 mice and might be a potential therapeutic target.

Ontario’s stroke prevention strategy appears to have had an unexpected, beneficial side effect: a reduction also in the incidence of dementia among older seniors. A new paper is the first to look at the demographics of both stroke and dementia across Ontario since the province pioneered Canada’s first stroke prevention strategy in 2000.

Human trials coming soon, results expected in 2-3 years, what is there not to like? A novel approach that has been done before but had some disadvantages. The researchers are now confident they have figured out the correct way to stop memory degeneration.